Human Atrial Natriuretic Peptide

Espiner, Eric A.; Nicholls, M. Gary

doi:10.1111/j.1365-2265.1987.tb00820.x

Cited by 39 publications

(18 citation statements)

References 83 publications

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“…The changes in blood pressure during ANF infusion alone may indicate a decrease in blood volume during ANF infusion, possibly due to a shift of fluid from the intravascular to the interstitial space, as recently reviewed by Espiner and Nicholls. 3 The failure of heart rate to rise does not fit this theory, but it may be due to an interference of ANF with sympathetic tone, as observed by Holtz et al 22 in the dog.…”

Section: Discussionmentioning

confidence: 88%

“…It has an immediate natriuretic effect, 4 -5 but it also inhibits aldosterone synthesis in vitro 6 -7 and in vivo. 3 -3 - 8 However, it is controversial whether the effect of ANF on aldosterone secretion occurs with near-normal plasma concentrations of the cardiac peptide and whether the effect in vivo is more or less mediated by changes in plasma renin levels. 9 -11 In the present study, we attempted to find a threshold dose of infused ANF that significantly affects aldosterone and renin secretion in sodium-deprived normal men.…”

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confidence: 99%

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Effects of incremental infusions of atrial natriuretic factor on aldosterone, renin, and blood pressure in humans.

1988

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SUMMARY To evaluate the physiological effects of human atrial natriuretic factor-(99-126) (ANF), we infused ANF, 0.1, 0.3, and 1.0 /ig/min, or placebo for 125 minutes on different days into six sodium-deprived normal men. During the last 45 minutes of infusion, angiotensin II, 6 ng/kg/min, was infused. Blood pressure, heart rate, plasma concentrations of ANF, aldosterone, and cortisol, and plasma renin activity (PRA) were measured before and during infusion. Steady state mean plasma ANF levels during infusion were 26.2 (placebo), 68.8 (0.1 n% ANF/min), 221 (0.3 ng ANF/min), and 648 pg/ml (1.0 /ig ANF/min). Systolic blood pressure fell significantly (with 1.0 /xg ANF/min), and diastolk pressure tended to rise in a dose-dependent manner, while heart rate was unchanged. PRA and plasma aldosterone fell during ANF infusion in a dose-dependent manner (significant with 0. A TRIAL natriuretic factor (ANF) may be phys-Z.\ iologically and pathophysiologically in-J-\~ volved in ridding the body of a sodium load and in preventing central venous pressure from rising above a certain limit.1 Most of the ANF activity in human plasma seems to be due to human However, it is controversial whether the effect of ANF on aldosterone secretion occurs with near-normal plasma concentrations of the cardiac peptide and whether the effect in vivo is more or less mediated by changes in plasma renin levels. 9 -11 In the present study, we attempted to find a threshold dose of infused ANF that significantly affects aldosterone and renin secretion in sodium-deprived normal men. Subjects and Methods Six healthy men (age range, 20-29 years; body weight range, 63-87 kg; mean body weight, 73.5 ± 8.5 kg) consented to participate in the study, the protocol of which had been approved by the ethical committee of Klinikum Steglitz (Berlin, West Germany). They were studied on 4 different days (three doses of ANF, one placebo infusion) within two periods of sodium depletion, during which the men collected their urine for the calculation of sodium and potassium balances. Sodium losses were induced to facilitate studying a possible suppressive effect of ANF on elevated basal renin and aldosterone levels. A period of sodium depletion consisted of 3 days on a low sodium diet (15 mmol sodium, 70 mmol potassium per day) plus a single 40-mg dose of furosemide (Lasix, Hoechst) on the morning of the first day. Therefore, most of the sodium loss occurred during the first 24 hours of the sodium depletion period, and the cumulative negative sodium balance at the end of Day 3 was not much different from that on the morning of Day 2. Infusion of one dose of ANF or placebo was given in the afternoon on Days 2 and 3. After an interval of 3 weeks on a free diet, the procedure of sodium depletion was

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Section: Discussionmentioning

confidence: 88%

mentioning

confidence: 99%

Effects of incremental infusions of atrial natriuretic factor on aldosterone, renin, and blood pressure in humans.

1988

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“…This hormone is released from the atrial granules in response to distension of the atria (Vollmar 1990) and has been shown to increase in the circulation in response to dynamic exercise (Perrault et al 1991(Perrault et al , 1994. Although the half life of ANP is quite short (2±3 min), it has been suggested that its haemodynamic eects persist for several hours (Espiner and Nicholls 1987). Several mechanisms may be responsible for its release during exercise, but it is generally accepted that these are secondary to the ANP release caused by the atrial distension imposed by increase in venous return (e.g.…”

Section: Introductionmentioning

confidence: 99%

Hypotension following mild bouts of resistance exercise and submaximal dynamic exercise

MacDonald

MacDougall

Interisano

et al. 1999

European Journal of Applied Physiology

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Our purposes were (1) to examine resting arterial blood pressure following an acute bout of resistance exercise and submaximal dynamic exercise, (2) to examine the effects of these exercises on the plasma concentrations of atrial natriuretic peptide ([ANP]), and (3) to evaluate the potential relationship between [ANP] and post-exercise blood pressure. Thirteen males [24.3+/-(2.4) years] performed 15 min of unilateral leg press exercise (65% of their one-repetition maximum) and, I week later, approximately 15 min of cycle ergometry (at 65% of their maximum oxygen consumption). Intra-arterial pressure was monitored during exercise and for 1 h post-exercise. Arterial blood was drawn at rest, during exercise and at intervals up to 60 min post-exercise for analysis of haematocrit and [alphaANP]. No differences occurred in blood pressure between trials, but significant decrements occurred following exercise in both trials. Systolic pressure was approximately 20 mmHg lower than before exercise after 10 min, and mean pressure was approximately 7 mmHg lower from 30 min onwards. Only slight (non-significant) elevations in [alphaANP] were detected immediately following exercise, with the concentrations declining to pre-exercise values by 5 min post-exercise. We conclude that post-exercise hypotension occurs following acute bouts of either resistance or submaximal dynamic exercise and, in this investigation, that this decreased blood pressure was not directly related to the release of alphaANP.

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“…The excitement and intensity of effort generated by their discovery is without precedent in modern biological science. Within 4 years of the original report of De Bold et al [2], the amino acid sequence of the active circulat ing peptide as well as its prohormone and prehormone forms were elucidated, together with their gene structure and target tissue receptor characteristics [3][4][5][6][7][8][9][10][11][12][13][14][15]. Evi dence regarding postreceptor events, especially the acti vation of particulate guanylate cyclase, implies a critical role for cyclic guanosine monophosphate (cGMP) as the second messenger responsible for many of the actions of atrial peptides: vasorelaxation, natriuresis, diuresis, in hibition of adrenal aldosterone biosynthesis, and a trans location of fluid from the vascular into the interstitial compartment.…”

Section: Introductionmentioning

confidence: 99%

Effects of Water Immersion on Atrial Natriuretic Peptide Release in Humans

Epstein

Norsk²,

Loutzenhiser³

1989

Am J Nephrol

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Water immersion (WI) to the neck induces prompt increases in central blood volume, central venous pressure, and atrial distension. Since atrial distension is a major stimulus for atrial natriuretic peptide (ANP) release, WI constitutes a unique model to investigate the physiological importance of ANP in humans. All studies to date demonstrate that ANP increases during the 1st h of WI in hydrated subjects, rising 2.5- to 3-fold by the end of the 2nd or 3rd h. During recovery from WI, ANP returns promptly to prestudy levels. Although distension of the atria probably constitutes the major stimulus for ANP release during WI, other mechanisms may coexist. In normal hydrated subjects undergoing WI, the increases in ANP correlate with the magnitude of the natriuresis, suggesting that ANP constitutes an important determinant of renal sodium handling in humans. It is simplistic, however, to consider the Wl-induced augmentation of ANP to be the sole, or even the prepotent, mediator of the resultant natriuresis. Rather ANP should be considered as one of several hormonal, neural, and hemodynamic factors acting in concert in an integrated matrix to modulate volume homeostasis. Clearly, the results of several recent studies utilizing WI demonstrate that this maneuver constitutes an important investigative model to delineate further the role of ANP in subserving volume homeostasis in normal humans and in disorders of deranged volume regulation.

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Human Atrial Natriuretic Peptide

Cited by 39 publications

References 83 publications

Effects of incremental infusions of atrial natriuretic factor on aldosterone, renin, and blood pressure in humans.

Effects of incremental infusions of atrial natriuretic factor on aldosterone, renin, and blood pressure in humans.

Hypotension following mild bouts of resistance exercise and submaximal dynamic exercise

Effects of Water Immersion on Atrial Natriuretic Peptide Release in Humans

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